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Blood, 15 February 2001, Vol. 97, No. 4, pp. 867-874
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Rising pp65 antigenemia during preemptive anticytomegalovirus
therapy after allogeneic hematopoietic stem cell transplantation: risk
factors, correlation with DNA load, and outcomes
W. Garrett Nichols,
Lawrence Corey,
Ted Gooley,
W. Lawrence Drew,
Richard Miner,
Meei-Li Huang,
Chris Davis, and
Michael Boeckh
From the Fred Hutchinson Cancer Research Center Program
in Infectious Diseases and the University of Washington, Seattle, WA;
and the Department of Laboratory Medicine, University of California,
San Francisco Medical Center, Mount Zion, San Francisco, CA.
To determine the risk factors and outcomes associated with rising
cytomegalovirus (CMV) antigenemia levels during preemptive therapy
among stem cell allograft recipients, 119 patients with CMV antigenemia
were studied. Patients were prospectively monitored for CMV antigenemia
weekly; those with positive findings on antigenemia tests were treated
with intravenous ganciclovir (5 mg/kg twice daily for 1 week, followed
by 5 mg/kg per day for 5-6 d/wk). While on therapy, 47 of 119 (39%)
patients demonstrated increases that were 2 or more times greater than
their baseline values, whereas 33 of 119 (28%) patients demonstrated
increases that were 5 or more times greater. Rising antigenemia was
confirmed by polymerase chain reaction for CMV DNA. Multivariate
analysis identified corticosteroids as the primary risk factor for
increasing antigenemia: for increases greater than or equal to twice
the baseline, 1 to 2 mg/kg steroids was associated with an odds ratio
(OR) of 4.0. For increases greater than or equal to 2 mg/kg steroids,
the OR was 10.1. CMV isolates obtained at the time of rising
antigenemia were susceptible to ganciclovir, indicating that resistance
was not a major factor. Overall, rising antigenemia levels were not
correlated with CMV disease. All 4 patients in whom CMV disease
developed during therapy, however, had rising antigenemia levels. Among
the 47 patients with antigenemia increases greater than or equal to
twice the baseline, 15 were re-induced with antivirals, whereas 32 continued to receive maintenance therapy. All 4 patients in whom CMV
disease developed during therapy received maintenance therapy, and 3 died with CMV disease. Thus, host factors such as the receipt of
corticosteroids explain increasing viral load during the early phase of
preemptive therapy. Continued induction dosing or re-induction may
protect against early breakthrough CMV disease and CMV-related death
among patients with rising antigenemia on preemptive therapy.
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